1. Field of the Invention
The present invention relates to an implantable gastric electrical stimulator system that can be used to decrease gastric motility and/or gastric efficiency for the treatment of obesity. More particularly, the system employs an implantable electrical stimulator, one or a plurality of implant-able stimulator leads (electrodes), and an external programmer, and an algorithm used to automatically control synchronized electrical stimulation frequency, interval, amplitude, or a combination of such parameters for treatment of obesity and other eating disorders.
2. Description of the Related Art
Obesity is a major health concern in western civilization. Surveys indicate that 33% of the population is overweight with the number increasing every year. Obesity is the second leading cause of preventable death in the United States. It is associated with several comorbidities that affect almost every body system. Some of these comorbidities are: hypertension, diabetes, coronary disease, breathing disorders, and musculoskeletal problems. It is estimated that the costs associated with obesity approach $70 billion per year.
Multiple factors contribute to obesity, but the two major factors are physical inactivity and overeating. Existing therapies include diet, exercise, appetite suppressive drugs, metabolism enhancing drugs, surgical restriction of the gastric tract, and surgical modification of the gastric tract. Efficacy of these therapies range from little or no weight loss up to weight loss approaching 50% of initial body weight.
Gastroparesis is an adverse medical condition in which normal gastric function is impaired. Gastroparetic patients exhibit reduced gastric motility with accompanying symptoms of nausea and/or vomiting and gastric discomfort. They may complain of bloating or a premature or extended feeling of fullness (satiety). Typically, the condition results in reduced food intake (in portion and/or frequency) and subsequent weight loss. Physiologically, the condition may be associated with damage or neuropathy of the stomach enervation or damage or dystrophy of the stomach muscle with subsequent attenuated (in amplitude and/or frequency) peristaltic activity of the stomach muscles. Some studies indicate that it is also associated with dysrhythmias of the stomach.
An examination of the symptomology and consequences of gastro-paresis reveals some effects that could be beneficial as a therapy for obesity, if they could be mediated and modulated. This disclosure sets forth a class of implantable electrical device(s) that can potentially effect a mild, reversible form of gastroparesis by inducing electrophysiological disorganization or disruption in the normal stomach motility.
The stomach is a complex organ of the digestive tract (alimentary canal) with the primary functions of dissolution, reduction, and motility of ingested food. These typical functions are accomplished through secretion of biochemical reagents to promote dissolution; kinetic mixing movements to reduce the particle size and promote mixing; and kinetic propulsive movements to move the chyme (solution of small food particles and biochemical reagents) into the intestines. The kinetic movements of the stomach are accomplished by organized/phased contractions of the stomach wall/smooth muscle.
Normal contractions of the stomach are the result of three control components: neural activity, chemical activity, and myogenic activity.
The neural control component refers to the intrinsic and extrinsic nerves innervating the stomach. The intrinsic nerves release various neurotransmitters and peptides that control contractions and motility. Studies indicate that the extrinsic nerves may influence the contractions by the release of modulative substances.
The chemical control component refers to the various substances (neurotransmitters, neuromodulators and peptides) released from the nerve endings or endocrine-paracrine cells and glands of the stomach. These biochemical substances may act directly on the smooth muscle cell or on the nerves to modulate or control the occurrence of contractions and motility.
The myogenic control component refers to small electrical oscillations of the smooth muscle cells related to polarization and depolarization of the smooth muscle cells. The myogenic activity is referred to as electrical control activity or slow waves.
The slow wave is the underlying clock for peristaltic activity. Slow waves are omnipresent and typically occur at frequencies of 2-4 cycles per minute. All slow waves are not linked to contractions, but a normal peristaltic contraction must occur in synchrony with a slow wave.
To initiate normal peristaltic contractions, multiple control means must be present. The slow wave (resulting from the cell membrane potential depolarization) provides the basic timing/interval and organization. However, the strength of the typical slow wave depolarization alone is not sufficient to exceed the excitation threshold required to initiate the smooth muscle contraction. A neural or chemical component must also be present to augment the myogenic activity. When a neural and/or chemical component is present, the depolarization strength exceeds the excitation threshold and a contraction occurs. (The contraction results in additional electrical activity referred to as electrical response activity or action potentials.)
However, initiating the contraction is only part of the peristaltic activity. To be physiologically effective (efficiently reduce, mix and/or propulse the stomach contents), the contraction must propagate in an organized, phased manner in three dimensions and in time (across and/or along the various muscle layers of the stomach).
Typically, the contraction involves the circular and longitudinal muscle layers of the stomach wall. Contraction of the circular smooth muscle layer decreases the lumen diameter. Contraction of the longitudinal muscle layer decreases the length of the stomach and may serve to assist in expansion of the lumen adjacent to the contracted circular muscle layer and to propagate the contraction to the neighboring uncontracted segment of the circular muscle. Coordinated contraction between both muscle layers is necessary for peristaltic propagation.
Intentional interference with any or all of the three control components and/or the coordination of the contraction propagation may impair the contraction and its associated kinetic function. Electrophysiologically, the interference may be administered as any one or combination of the following:
(a) electrical stimulation that induces asynchronous depolarization of individual cells or small groups of cells just prior to (spatially or temporally) or during a slow wave or peristaltic wave creating disorganization/attenuation of the wave;
(b) electrical stimulation that induces synchronous depolarization of a large area of cells prior to a slow wave or peristaltic wave creating an area that is refractory to the wave (may also induce a contraction);
(c) persistent electrical stimulation of the stomach nerves creating a neural desensitization, suppression or blocking of the stimulated area;
(d) electrical stimulation that entrains the slow wave at a frequency greater than 4 cpm creating a tachygastria condition so that peristalsis does not occur;
(e) electrical stimulation that entrains the slow wave at a frequency that competes with the intrinsic frequency but originates at a different location(s) creating competing ectopic waves; and
(f) temporally or spatially segregated, directional electrical stimulation of the individual muscle layers creating decoupling of the peristaltic coordination.
Additional methodologies may also accomplish the same ends, but may not be as easily applied, may require iterative or multiple applications or may be difficult to reverse. These additional methods include:
(a) creation of gastric smooth muscle lesions by ablative techniques (radio frequency, microwave, cryogenic) to lessen the contractility of the muscle or to change the contraction vector to a less efficient direction/sequence; and
(b) administration of precise doses and patterns of intramuscular paralytic agents (e.g. botulism toxin, curare, etc.) to prevent the affected areas from contracting and/or to force a contraction along a specific less efficient path.
These items are discussed in separate disclosures. This disclosure will focus on the electrophysiological means of impairment.
Electrical stimulation of the stomach and other portions of the gastric intestinal tract has been experimented with for some time. Most of the experimentation has been oriented toward improving the gastric emptying usually by attempting to speed up or strengthen/reinforce the peristaltic activity.
U.S. Pat. No. 5,423,872 to Cigaina for “Process and Device for Treating Obesity and Syndromes Related to Motor Disorders of the Stomach of a Patient” issued Jun. 3, 1995, describes an implantable gastric electrical stimulator at the antrum area of the stomach which generates sequential electrical pulses to stimulate the entire stomach, thereby artificially altering the natural gastric motility to prevent emptying or to slow down food transit through the stomach. Cigaina however has the inherent disadvantage that it is a stimulation device solely, and does not incorporate on-demand stimulation other than that of manual cycling provided by magnetic application, which wastes energy by applying stimulation when it is not therapeutically required.
U.S. Pat. No. 5,690,691 to Chen et al. for “Gastro-intestinal Pacemaker Having Phased Multi-Point Stimulation” issued Nov. 25, 1997, describes a portable or implantable gastric pacemaker employing a number of electrodes along the greater curvature of the stomach for delivering phased electrical stimulation at different locations to accelerate or attenuate peristaltic movement in the GI tract. Chen et al. additionally provides a sensor electrode or a stimulation electrode wherein the response of an organ to an electrical stimulation pulse is sensed for delivering stimulation to a plurality of electrodes to provide phased electrical stimulation. However, Chen et al. is specifically directed to phased stimulation that progresses through the plurality of electrodes located along the peristaltic flow path and specifically senses the response of the organ to the electrical stimulation. Chen does not address sensing of the intrinsic electrical activity for the purpose of applying therapy.
U.S. Pat. No. 5,836,994 to Bourgeois for “Method and Apparatus for Electrical Stimulation of the Gastrointestinal Tract” issued Nov. 17, 1998, describes an implantable gastric stimulator which incorporates direct sensing of the intrinsic gastric electrical activity by one or more sensors of predetermined frequency bandwidth for application or cessation of stimulation based on the amount of sensed activity. The Bourgeois sensing circuitry inhibits therapy if a peristaltic wave is sensed and provides stimulation if it is not sensed. It does not apply therapy to impair gastric motility.
U.S. Pat. No. 6,091,992 to Bourgeois for “Method and Apparatus for Electrical Stimulation of the Gastrointestinal Tract” issued Jul. 18, 2000, is similar to the '994 patent. It relates to provision of separate electrical pulse trains of differing parameters wherein the pulse trains are composed of a series of at least two pulses. The therapy is applied to promote gastric peristalsis.
U.S. Pat. No. 6,104,955 to Bourgeois for “Method and Apparatus for Electrical Stimulation of the Gastrointestinal Tract” issued Aug. 15, 2000, relates to a gastric stimulator with reversion to a sensing mode to determine the intrinsic slow wave interval to prevent stimulation when the gastric tract is in inter-digestive phases. Like the previous Bourgeois patents, '955 addresses stimulation to promote gastric normalcy.
U.S. Pat. No. 5,861,014 to Familoni for “Method and Apparatus for Sensing a Stimulating Gastrointestinal Tract On-Demand” issued Jan. 19, 1999, relates to an implantable gastric stimulator for sensing abnormal electrical activity of the gastrointestinal tract so as to provide electrical stimulation for a preset time period or for the duration of the abnormal electrical activity to treat gastric rhythm abnormalities. Familoni also addresses recording of abnormal activity for a preset time period, but does not address altering of a normal gastric activity to achieve a variable result such as treatment for obesity. It does not apply therapy to disrupt normal gastric activity.
Accordingly, the known prior art relates to (1) the provision of electrical stimulation (phased or unphased) without regard to intrinsic activity, or (2) the provision of electrical stimulation to induce normal peristalsis, or (3) the provision of electrical stimulation to counteract abnormal gastric activity.
Thus, the prior art does not address the provision of electrical stimulation with regards to intrinsic gastric electrical activity for the intended purpose of disrupting normal, intrinsic gastric activity.